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Titolo:
Direct presynaptic regulation of GABA/glycine release by kainate receptorsin the dorsal horn: An ionotropic mechanism
Autore:
Kerchner, GA; Wang, GD; Qiu, CS; Huettner, JE; Zhuo, M;
Indirizzi:
Washington Univ, Sch Med, Pain Ctr, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 d, Pain Ctr, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Anesthesiol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Anesthesiol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 & Neurobiol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA WashingtonUniv St Louis MO USA 63110 pt Psychiat, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USAWashington Univ St Louis MO USA 63110 l & Physiol, St Louis, MO 63110 USA
Titolo Testata:
NEURON
fascicolo: 3, volume: 32, anno: 2001,
pagine: 477 - 488
SICI:
0896-6273(20011108)32:3<477:DPROGR>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT SPINAL-CORD; SYNAPTIC TRANSMISSION; HIPPOCAMPAL INTERNEURONS; GABA RELEASE; GLUR6-DEFICIENT MICE; AMPA RECEPTORS; IN-VITRO; NEURONS; ACTIVATION; GLYCINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Zhuo, M Washington Univ, Sch Med, Pain Ctr, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Ctr, St Louis, MO 63110 USA
Citazione:
G.A. Kerchner et al., "Direct presynaptic regulation of GABA/glycine release by kainate receptorsin the dorsal horn: An ionotropic mechanism", NEURON, 32(3), 2001, pp. 477-488

Abstract

In the spinal cord dorsal horn, excitatory sensory fibers terminate adjacent to interneuron terminals. Here, we show that kainate (KA) receptor activation triggered action potential-independent release of GABA and glycine from dorsal horn interneurons. This release was transient, because KA receptors desensitized, and it required Na+ entry and Ca2+ channel activation. KA modulated evoked inhibitory transmission in a dose-dependent, biphasic manner, with suppression being more prominent. In recordings from isolated neuron pairs, this suppression required GABA(B) receptor activation, suggestingthat KA-triggered GABA release activated presynaptic GABA(B) autoreceptors. Finally, glutamate released from sensory fibers caused a KA and GABA(B) receptor-dependent suppression of inhibitory transmission in spinal slices. Thus, we show how presynaptic KA receptors are linked to changes in GABA/glycine release and highlight a novel role for these receptors in regulating sensory transmission.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/01/20 alle ore 18:53:59